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Cancer Dis:白血病治疗新方法让癌基因变“乏力”

2016-10-14 佚名 生物谷

一些基因的重新激活会导致造血干细胞发生异常自我更新从而发生白血病,这些与自我更新有关的基因发生异常激活可能由DNA包装过程中的一些结构性修饰引起。最近一项研究发现有两种染色质调节因子能够介导这些表观遗传修饰的变化,并且白血病细胞非常依赖这两种因子。来自美国的科学家取得了上述研究进展,他们证明利用靶向药使这两种染色质调节因子失活可以破坏白血病细胞的自我更新程序使白血病细胞发生逆转重新变成正常血细胞。


一些基因的重新激活会导致造血干细胞发生异常自我更新从而发生白血病,这些与自我更新有关的基因发生异常激活可能由DNA包装过程中的一些结构性修饰引起。最近一项研究发现有两种染色质调节因子能够介导这些表观遗传修饰的变化,并且白血病细胞非常依赖这两种因子。

来自美国的科学家取得了上述研究进展,他们证明利用靶向药使这两种染色质调节因子失活可以破坏白血病细胞的自我更新程序使白血病细胞发生逆转重新变成正常血细胞。相关研究结果发表在国际学术期刊Cancer Discovery上。

急性髓系白血病是一种恶性血液癌症,目前治疗这种疾病的主要方法是结合使用多种不同的化疗药物,但是由于病人基因型和年龄存在差异,只有大约一半的病人能够对这种治疗方法产生应答。

这项研究的目的在于开发更加有效毒性更小的治疗方法。最近研究表明DNA包装结构发生改变会促进癌症发育。这些化学修饰主要发生组蛋白上,组蛋白上的不同化学修饰会导致基因活性的上升或下降,而负责对组蛋白进行化学修饰的添加、阅读和移除的蛋白就叫做染色质调控因子。

该研究的主要研究对象是NPM1突变的AML亚型,这种亚型在60岁以下的成年白血病病人中非常常见。NPM1突变的AML亚型(NPM1mut白血病)与一类叫做HOX的干细胞基因的激活有关,HOX基因在发育过程中具有非常基础的作用,特别是对于造血干细胞的发育。虽然科学家们认为HOX基因激活会启动类似干细胞的自我更新,将正常血细胞变成白血病细胞,但是对于这类基因如何激活仍然不了解。

为了回答这一问题,研究人员利用CRISPR/CAS9技术,精确操作白血病细胞的DNA序列分析了MLL和DOT1L这两个蛋白的功能。通过实验证实,NPM1mut白血病细胞的存活依赖这两种蛋白的作用。这两个蛋白是控制染色质结构的重要调节因子,利用药物分别阻断这两个蛋白的活性能够降低NPM1mut白血病细胞中HOX干细胞基因的活性,同时阻断两个蛋白的活性能够使HOX干细胞基因的活性发生完全失活,白血病细胞也会发生实质性变化,开始变成正常血细胞。

这项研究代表了逆转白血病发生过程中一个关键机制实现靶向治疗NPM1突变型AML亚型的希望,也为未来进行临床试验提供了重要临床前研究基础。

原始出处

M. W. M. Ku hn, E. Song, Z. Feng, A. Sinha, C.-W. Chen, A. J. Deshpande, M. Cusan, N. Farnoud, A. Mupo, C. Grove, R. Koche, J. E. Bradner, E. de Stanchina, G. S. Vassiliou, T. Hoshii, S. A. Armstrong.Targeting Chromatin Regulators Inhibits Leukemogenic Gene Expression in NPM1 Mutant Leukemia.Cancer Dis.2016

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    2016-10-16 徐岩
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    2016-10-16 1e0ece0dm09(暂无匿称)

    谢谢分享学习

    0

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    2016-10-15 drmike

    这白血病急需有效的治疗!

    0

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    2016-10-15 Carlos007

    白血病很重要

    0

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    2016-10-15 半夏微凉

    学习了,继续关注!

    0

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